Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue.
There is no sensation of pain or discomfort, the muscle appears to simply ‘stop listening’ and gradually cease to move, often lengthening.
Part of the process of strength training is increasing the nerve's ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force.
It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit.
Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force.
[citation needed] Central fatigue is a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output.
[3][4][5] It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity.
[6][7] There has been a great deal of interest in the role of serotonergic pathways for several years because its concentration in the brain increases with motor activity.
[citation needed] Muscle cells work by detecting a flow of electrical impulses from the brain which signals them to contract through the release of calcium by the sarcoplasmic reticulum.
ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model.
Contrary to common belief, lactic acid accumulation does not actually cause the burning sensation we feel when we exhaust our oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce pyruvate in the liver which is known as the Cori cycle.
[citation needed] Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions.
This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions.